U.S. Pat. No. 9,067,071 (the '071 patent), U.S. application Ser. No. 14/642,699, filed Mar. 9, 2015 (the “699 application”), U.S. application Ser. No. 14/801,560, filed Jul. 16, 2015 (the “'560 application”), U.S. application Ser. No. 14/820,536, filed Aug. 6, 2015 (the “'536 application”), and U.S. application Ser. No. 15/098,237, filed Apr. 13, 2016 describe systems which may be used for hemodynamic control in the acute hospital care setting, by transvascularly directing therapeutic stimulus to parasympathetic nerves and/or sympathetic cardiac nerves using one or more therapeutic elements (e.g. electrodes or electrode arrays) positioned in the neighboring vasculature. Each of the above-referenced applications is incorporated herein by reference.
In accordance with a method described in the '071 patent, autonomic imbalance in a patient may be treated by energizing a first therapeutic element disposed in the vasculature to deliver therapy to a parasympathetic nerve fiber such as a vagus nerve and energizing a second therapeutic element disposed in the vasculature to deliver therapy to a cardiac sympathetic nerve fiber. Delivery of the parasympathetic and sympathetic therapy decreases the patient's heart rate (through the delivery of therapy to the parasympathetic nerves) while at the same time elevating or maintaining the blood pressure (through the delivery of therapy to the cardiac sympathetic nerves) of the patient in treatment of heart failure. For treatment of acute heart failure syndromes, the neuromodulation therapy may be used to lower heart rate and increase cardiac contractility.
The '071 patent describes a neuromodulation system having a parasympathetic therapy element adapted for positioning within a blood vessel, a sympathetic therapy element adapted for positioning with the blood vessel; and a stimulator configured to energize the parasympathetic therapy element to deliver parasympathetic therapy to a parasympathetic nerve fiber disposed external to the blood vessel and to energize the sympathetic therapy element within the blood vessel to deliver sympathetic therapy to a sympathetic nerve fiber disposed external to the blood vessel. In other methods of transvascular nerve capture, including some described in the '699 and '560 applications, therapy may be delivered using multiple therapeutic elements positioned in different blood vessels. For example, one therapeutic element may be positionable within a first blood vessel to capture a first nervous system target outside the first blood vessel, and the other may be positionable in a second, different, blood vessel to capture a second nervous system target outside the second blood vessel.
A neuromodulation system used for the therapy may include an external pulse generator/stimulator that is positioned outside the patient's body. The therapeutic elements may be carried by one or more percutaneous catheters that are coupled to the external pulse generator. In other embodiments an implantable stimulator may instead be used, in which case the therapeutic elements may be disposed on leads electrically coupled to the implantable stimulator/pulse generator. The stimulator/pulse generator is configured to energize the therapeutic elements to transvascularly capture the target nerve fibers.
Left ventricular contractility (“LV contractility” or “LVC”) is the strength and vigor with which the left ventricle of the heart contracts during systole. The greater the contractility the greater the stroke volume of blood per contraction of the heart. Since cardiac output (“CO”) is the product of stroke volume and heart rate, greater contractility of the left ventricle correlates to greater cardiac output (“CO”).
Left ventricular relaxation (“LV relaxation” or “LVR”) is the relaxation of the muscle of the left ventricle during diastole. Rapid relaxation of the left ventricle is important for proper functioning of the heart. It helps to draw blood into the ventricle and allows more complete filling of the left ventricle. Slow LVR can cause congestion and thus increased pressure in the pulmonary circuit, and insufficient filling of the left ventricle. Some medical conditions, such as heart failure with preserved ejection fraction, can result in a reduction of LVR. Some treatments may cause an increase in contractility without causing a corresponding increase in relaxation. For example, heart failure patients are often treated using administration of inotropes, a treatment that increases contractility with the goal of increasing cardiac output, but because they do not cause a corresponding increase in relaxation, the left ventricle may not be able to fill adequately and cardiac output can remain compromised.